2023 Study: Nattokinase Degrades Alzheimer's Plaques in Animal Model
In the battle against Alzheimer's disease, an unexpected ally has recently emerged in the form of Nattokinase, an enzyme derived from fermented soybeans. A 2023 study has found that Nattokinase directly targets and breaks down harmful plaques associated with Altheimer’s Disease. This remarkable compound, which has long been known to break down blood clots, and has more recently gained notoriety for its ability to dissolve the COVID-19 spike protein, appears to hold promise in the field of neurodegenerative disease as well.
What is Alzheimer’s Disease?
Alzheimer's disease (AD) is the most common form of dementia, affecting more than 55 million people worldwide. As the global population continues to age, researchers expect this number to triple by 2050.
AD is characterized by the accumulation of harmful substances known as amyloid-beta plaques within the brain. These plaques have a destructive effect on brain cells and are thought to play a central role in triggering symptoms such as progressive memory loss, cognitive decline, and changes in behavior and personality.
The Role of Amyloid Beta
Amyloid-beta peptides have long been viewed as a signature of Alzheimer’s pathology. When these peptides aggregate (clump together), they form insoluble plaques in the brain that are toxic to neurons (brain cells). These aggregates can disrupt communication between neurons and instigate inflammatory responses that result in cell damage and death. While there is significant controversy among scientists regarding the role of amyloid in the disease, its clearance has been a central target of therapeutics in the research over the past few decades.
Nattokinase Degrades Amyloid-Beta
In this quest to treat Alzheimer's, researchers have been exploring the properties of a natural enzyme called nattokinase. Originating from a Japanese dish called natto, made from fermented soybeans, nattokinase has traditionally been recognized for its cardiovascular benefits due to its ability to break down blood clots. More recently, it has been lauded for its capacity to dissolve the COVID-19 spike protein.
A 2023 study out of a lab in China found that nattokinase is capable of breaking down harmful forms of amyloid beta both in vitro (in a petri dish/test tube) and in vivo (in an animal model). When given orally to mice for 14 days, amyloid concentration was significantly reduced in both the bloodstream and the brain over time. The researchers conclude that given its safety profile and positive effects, “[Nattokinase] may be potentially developed as an anti-Aβ42/Aβ40 drug for the prevention, treatment, and long-term care of [Alzheimer’s Disease.]”
Earlier research, back in 2013, suggested that Nattokinase not only degrades harmful plaques, but also dampens the inflammatory response, and promotes the proliferation of neuroprotective molecules such as brain-derived neurotrophic factor. Some of its benefits, researchers propose, also come from its capacity to scavenge harmful free radicals.
Alzheimer's disease is a poorly understood, multifaceted condition, making effective treatments challenging to develop. Further studies will be required to highlight the exact mechanisms by which nattokinase interacts with amyloid-beta aggregates and to explore possible side effects and optimum dosages for potential therapeutic use. If these further studies are successful, the implications could be meaningful in the fight against Alzheimer's.
While the road to an Alzheimer's cure is anything but clearcut, the introduction of nattokinase into the medical community's arsenal is a significant development that if nothing else, warrants further study, and underscores the remarkable effects of this natural compound.
Ni, A., Li, H., Wang, R., Sun, R., & Zhang, Y. (2023). Degradation of amyloid β-peptides catalyzed by nattokinase in vivo and in vitro. Food Science and Human Wellness, 12(5), 1905-1916.
Fadl, N. N., Ahmed, H. H., Booles, H. F., & Sayed, A. H. (2013). Serrapeptase and nattokinase intervention for relieving Alzheimer’s disease pathophysiology in rat model. Human & experimental toxicology, 32(7), 721-735.